Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “coding variants”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,207 records · Page 67Linked to original sources

Possible association of a silent polymorphism in the neuronal nicotinic acetylcholine receptor subunit alpha4 with common idiopathic generalized epilepsies.

The alpha4 subunit gene of the neuronal nicotinic acetylcholine receptor (CHRNA4) has recently been identified as the first gene underlying an idiopathic partial epilepsy syndrome in human, autosomal-dominant nocturnal frontal lobe epilepsy (ADNFLE). CHRNA4 is located in the candidate region for benign familial neonatal convulsions and low-voltage EEG on chromosome 20q. In the present study, we examined the possible role of CHRNA4 in common subtypes of idiopathic generalized epilepsy (IGE), comprising childhood and juvenile absence epilepsy and juvenile myoclonic epilepsy (JME), by systematically screening the coding region of the gene for sequence variants. We present here a population-based association study testing the hypothesis that variants of the CHRNA4 gene confer genetic susceptibility to common subtypes of IGE. The missense mutation (Ser248Phe), associated with ADNFLE, and four silent polymorphisms in the CHRNA4 gene were genotyped in 103 IGE patients and 92 controls by polymerase chain reaction and subsequent restriction analysis. Without correction for multiple testing, the frequency of the T-allele of the silent CfoI bp595 polymorphism was increased in the entire group of IGE patients (f(T) = 0.085) compared to that in the controls (f(T) = 0.027). The allelic association was not restricted to any subgroup of IGE with either JME or idiopathic absence epilepsies. This result suggests that variation of the CHRNA4 gene, or so-far-undetected sequence variants near the CHRNA4 locus, confer susceptibility to the common IGE syndromes.

Alleles↗

Vascular endothelial growth factor expression in early stage ovarian carcinoma.

BACKGROUND: Tumor angiogenesis is essential for solid tumor growth. Yet, the importance of any particular factor in neoplastic proliferation is poorly defined. This study examines the clinical significance of increased expression of one of the angiogenic factors, vascular endothelial growth factor (VEGF), in early stage ovarian carcinoma. METHODS: Tumor specimens from 68 patients with International Federation of Gynecology and Obstetrics Stage I and II ovarian carcinoma were evaluated for VEGF expression. Antisense and corresponding sense (control) RNA probes were transcribed from the pCRII construct (Invitrogen, San Diego, CA), which contained human VEGF cDNA. The antisense probe was designed to include a highly conserved region of the VEGF coding sequence and thus detect all known variants. After in situ hybridization, sections were assessed for overexpression of VEGF. RESULTS: Twenty-nine of the tumor samples overexpressed VEGF, whereas 39 specimens did not. In patients whose tumors demonstrated elevated VEGF expression, 25% were without evidence of disease recurrence at last follow-up. In contrast, 75% of the patients whose tumors did not overexpress VEGF were without evidence of disease at last follow-up (P < 0.001). Median disease free survival for the VEGF positive group was 22 months, compared with > 108 months for the VEGF negative group (P < 0.001). When borderline tumors were excluded from the survival analysis, median disease free survival for the VEGF positive group was 18 months, compared with >120 months for the VEGF negative group (P < 0.001). Other possible prognostic variables had minimal impact on survival; these included age, stage, grade, cytology, and tumor size (P > 0.05). Assignment to a high risk group, as defined by the Gynecologic Oncology Group of the National Cancer Institute, was somewhat predictive of a shorter relapse free interval (P = 0.056). In a multivariate analysis, however, only elevated VEGF expression was associated with poorer survival. CONCLUSIONS: In this analysis, patients with early stage ovarian carcinoma with increased VEGF expression had a poorer prognosis. Further study of VEGF may ultimately lead to identification of patients with high risk lesions whose tumor biology portends a worse prognosis and who therefore may benefit from aggressive adjuvant therapy.

Adult↗

Cluster of genes encoding the major egg envelope protein of zebrafish.

The proteins of fish egg envelopes are encoded by genes that are closely related to the genes for human zona pellucida proteins. A cluster of three genes coding for an egg envelope protein was isolated from the zebrafish, Danio rerio. The three genes, zp2a, zp2b, and zp2c, are located within an 11 kb region and are each comprised of eight exons spanning 1.85 kb. The exon-intron structures of the genes are nearly identical; however, their deduced amino acid sequences diverge at exon 7 (zp2b and zp2c from zp2a) and exon 8 (zp2c from zp2b). Exons 2-7 have a structural organization similar to exons in the carboxy-terminal half of the human zona pellucida ZP1, ZP2, and ZPB genes, suggesting they arose from a common ancestral gene. Sequence comparisons indicate that the deduced zebrafish proteins are most closely related to human ZPB. Zebrafish mRNAs coding for each of the three ZP2 variants have been found either as full-length cDNAs or expressed sequence tags. Distinct from the wf(female) gene of winter flounder which we first reported (Lyons et al., 1993: J Biol Chem 268:21351-21358), expression of the zebrafish zp2 genes was found to be ovary-specific, instead of liver-specific, and the promoter regions of zp2a and zp2b, while different, both contained E-box sequences (CANNTG) that have been demonstrated to be essential for coordination of zona pellucida gene expression in mammalian oocytes. Mixed peptide sequence analysis was used to identify the major polypeptide component of isolated zebrafish egg envelopes as the zp2 gene product.

Amino Acid Sequence↗

C1q binding to chimeric monoclonal IgG3 antibodies consisting of mouse variable regions and human constant regions with shortened hinge containing 15 to 47 amino acids.

We have constructed four different deletion mutants of a chimeric mouse-human IgG3 anti-(4-hydroxy-3-nitrophenyl)acetyl/(5-iodo-4 hydroxy-3 nitrophenyl) acetyl (NP/NIP) antibody lacking one or more of the four exons coding for the hinge region. The mutant variants all retained intact hinge region epitopes since they all reacted with IgG3 hinge-specific antibodies. Surprisingly, all the deletion mutants bound C1q equally well or even better than the wild type. Thus the high C1q binding activity of IgG3 compared to IgG1 is apparently not due to the total length of the IgG3 hinge, which is 62 amino acids, nor is it due to the length of the upper hinge which is the stretch from the end of CH1 to the first inter-heavy chain disulfide bond.

Amino Acid Sequence↗

Genetic variation of hepatitis B surface antigen coding region among infants with chronic hepatitis B virus infection.

Variants in the amino acid composition of the primary antibody-binding site of hepatitis B surface antigen (HBsAg) have been identified in a number of populations with chronic hepatitis B virus (HBV) infection. Direct sequencing of amplified or cloned PCR products, solid phase detection of sequence-specific PCR products (SP-PCR), and limiting dilution cloning PCR (LDC-PCR) were compared to determine their sensitivity in detecting differing concentrations of HBsAg variants. LDC-PCR had the greatest sensitivity and could detect HBsAg variants at a concentration of 0.1% of the total viral population. HBsAg variants were detected in 51% of infants with chronic HBV infection acquired after postexposure prophylaxis, and more than half of the variants were detected only by the most sensitive methods.

Cloning, Molecular↗

The chromosome 9q genes TGFBR1, TSC1, and ZNF189 are rarely mutated in bladder cancer.

This study assessed a series of bladder tumours and bladder tumour cell lines for sequence variation in the Krüppel-like zinc finger gene ZNF189, the tuberous sclerosis complex gene 1 (TSC1), and the TGF beta receptor type I (TGFBR1). All three genes have been mapped to 9q regions commonly deleted in transitional cell carcinoma of the bladder. Mutation analysis of the coding sequence of these genes revealed several variant bands that were shown to represent polymorphisms. Mutation analysis of the ZNF189 gene in bladder cancer cell lines identified one amino acid substitution (lysine-->isoleucine) at position 323 in exon 4. For the TSC1 gene, two mutations were identified in two out of 27 independent cell lines. Both mutations result in a truncated protein. Furthermore, one out of 36 bladder tumours had a frameshift mutation in exon 7 of the TSC1 gene. No tumour-specific mutations were found in the TGFBR1 gene. The length of the polyalanine tract present in exon 1 of the TGFBR1 gene was also investigated. It has been suggested that the allele with six alanines (6A) is more frequent in patients with bladder and other cancers, so bladder cancer patients were compared with normal controls. In both groups, the percentage of heterozygotes was 17%. These data do not support a role for the 6A allele in bladder cancer susceptibility.

Activin Receptors, Type I↗

Genomic organization and tissue-specific expression of splice variants of mouse organic anion transporting polypeptide 2.

cDNAs that code for mouse organic anion transporting polypeptide 2 (oatp2) have been cloned. At least three forms of mouse oatp2 cDNAs containing the same coding sequence were isolated. The common coding sequence is for a protein of 670 amino acids with 12 putative transmembrane domains. The deduced amino acid sequence of the mouse oatp2 shares 89% identity with the reported rat oatp2. Cloning and analysis of mouse oatp2 gene indicates that these isoforms are alternatively spliced products from the same gene. Heterogeneity was observed in the 5'-untranslated region of the cDNAs. Two of the three isoforms lacked the noncoding exon 3 sequence. Northern-blot hybridization analysis using the exon 3-specific probes demonstrated that mouse oatp2 mRNA containing exon 3 sequence is expressed in heart and lung, whereas exon 1-, 2-, and 17-specific probes detected mRNA only in brain and liver. The mouse oatp2 gene consists of 17 exons, including three noncoding exons, and 16 introns. All of the introns are flanked by GT-AG splice sequences except for intron 10 that is flanked by GC-AG splice sequence.

Alternative Splicing↗

ABCA6, a novel a subclass ABC transporter.

Here we report the cDNA cloning of a novel member of the ABC A transporter subfamily from human macrophages. The identified coding sequence is of 5.0 kb size and contains an open reading frame which encodes a 1617 amino acid polypeptide. Structurally, the putative ABC transporter protein product consists of two tandemly oriented subunits, each composed of a transmembrane domain followed by a nucleotide binding fold, and thus conforms to the group of full-size ABC transporters. We also demonstrate the existence of an alternative transcript that codes for a 637 amino acid protein variant bearing the features of a truncated half-size transporter. Among the human ABC transporter subfamily A the novel transporter shows highest protein sequence homology with ABCA8 (60%), followed by ABCA2 (32%) and ABCA1 (32%), respectively. In agreement with the proposed classification, the novel transporter was designated ABCA6. The ABCA6 gene is ubiquitously expressed with highest mRNA levels in liver, lung, heart and brain. Analysis of the genomic organization demonstrated that the ABCA6 gene is composed of 38 exons which extend across a region of 62 kb size on chromosome 17q24.2. Based on its structural features and its cholesterol-responsive regulation ABCA6 is potentially involved in macrophage lipid homeostasis.

ATP Binding Cassette Transporter 1↗

Immunoscreening of a cutaneous T-cell lymphoma library for plasma membrane proteins.

Cutaneous T-cell lymphomas (CTCL) belong to non-Hodgkin lymphomas, which are primarily manifested in the skin and mostly exhibit a T-helper memory phenotype. Mycosis fungoides (MF) and the leukemic variant Sézary syndrome (SzS) are the most common forms of CTCL. The aim of this study was to identify CTCL surface proteins with a tumor specific expression profile. A plasma membrane enriched fraction of the CTCL cell line HuT78 was used for immunization of two rabbits. Subsequently, a CTCL cDNA phage library was screened by a new variant of the SEREX method (serological identification of antigens by recombinant expression cloning) using the polyspecific rabbit antisera instead of patients' sera. Isolated reactive transfectants were sequenced and 42 different genes identified including four known plasma membrane proteins: Ligatin, HLA-A, integrin alpha4 and MT5-MMP. The level of transcripts of the matrix metalloproteinase MT5-MMP was diminished in MF tumor specimens. MT5-MMP normally occurs in several different protein variants. Western blot analysis revealed that activated MT5-MMPs were reduced in tumor specimens, whereas the amounts of most of the inactivated variants were unchanged. The amount of mRNA coding for the adhesion protein integrin alpha4 was not altered in tumor specimens in comparison to controls when analyzed by quantitative real-time PCR analysis. Ku86, known to be predominantly located in the nucleus and cytosol, was frequently detected during the SEREX screening. Western blot analysis revealed higher protein amounts of Ku86 in HuT78 than in control cells. In addition, we could show, that Ku86 can also be detected in lipid rafts of CTCL cells as it has been described for other tumor types. Thus, Ku86 might be involved in homo- and heterotypic adhesion steps of CTCL tumor cells and might protect these cells against apoptosis triggered by irradiation as it was suggested for multiple myeloma cells. The design of this study enabled screening for all proteins on the plasma membrane, irrespectively of whether these are directly anchored within the membrane or associated with other membrane proteins. Further analysis will unravel whether the list of identified proteins harbors candidates, which might be accessible for antibodies from outside the cell.

Animals↗

Human endothelial cells allow passage of an archetypal BK virus (BKV) strain--a tool for cultivation and functional studies of natural BKV strains.

The ubiquitous human polyomavirus BK (BKV) causes the serious condition BKV-nephropathy in an increasing number of renal-transplant patients. The lack of authentic cell cultures for multiplication of naturally occurring strains has hampered cultivation and functional studies of BKV. Here we demonstrate that the most common urine shed BKV strain, the archetype, multiplies in the human endothelial cell line HUV-EC-C. Additional variants with deletions in the non-coding control region (NCCR) appear upon prolonged propagation. Although the titer produced was low, at the present HUV-EC-C is the only cell line shown to allow propagation of archetypal BKV. HUV-EC-C may therefore be a useful tool for BKV cultivation as well as functional studies.

BK Virus↗

Heterogeneity of three electrophoretically distinct Go alpha-subunits in mammalian brain.

So far three splice variants of the alpha o-gene coding for two alpha o proteins have been identified by molecular cloning, and the corresponding proteins purified. In the present study subtype-specific peptide antibodies revealed the existence of an electrophoretically distinct third form of alpha o in mammalian brain membranes which migrates more slowly on SDS-PAGE and shows a more acidic pI value than the other alpha o-subunits. Each of the three alpha o-subunits is detected as two isoforms when enriched from brain membranes. Rodent alpha o-subunits differ from non-rodent species in their electrophoretic mobilities. The results suggest that (i) there may exist a novel alpha o-subunit which reacts with an alpha o1-subunit-specific antibody, (ii) each alpha o-subunit may exist in more than one co- or posttranslationally modified isoform in brain membranes, and (iii) differences between alpha o-subunits from different species exist which are detectable by gel electrophoretic methods.

Amino Acid Sequence↗

Control of reovirus messenger RNA translation efficiency by the regions upstream of initiation codons.

The 10 species of reovirus messenger RNA are translated in vivo with efficiencies/frequencies that differ by as much as 100-fold. The s1 mRNA, which is translated 10 times less efficiently than the s4 mRNA but 10 times more efficiently than the/1 and m1 mRNAs, has a unique BamH1 cleavage site located immediately downstream of its initiation codon. Because the reovirus mRNAs have been cloned, this provides the opportunity for placing modified and altered sequences upstream of its coding sequence. The translation efficiencies of the variant mRNAs, transcribed via the SP6 in vitro transcription system, can then be measured in the rabbit reticulocyte lysate in vitro translation system. Using this system it was found that replacing the 5'-upstream sequence of the s1 mRNA with that of the s4 mRNA increases its in vitro translation efficiency by 4-fold; that the trinucleotide immediately upstream of the s1 initiation codon renders it very weak, and that it is only slightly superior to the weakest Kozak consensus sequence; that the nature of the nucleotides further upstream than position -3 can profoundly affect translation efficiency; that the nature of this effect is in turn markedly modified by the nature of nucleotides in positions -1 to -3; and that there is a minimum optimal 5'-upstream sequence length of about 14 nucleotides. We also investigated the effect of secondary structure involvement on the ability of 5'-upstream sequences to promote translation. Two effects were noted. First, being part of moderately stable stem loops (delta G, -18 kcal/mol) decreased translation efficiency about 3-fold; second, mRNA in which only three 5'-terminal nucleotides were unpaired were translated five times less efficiently than mRNA in which six nucleotides were unpaired. Accessibility of the 5'-cap as well as secondary structure of the 5'-upstream sequences are therefore factors that affect translation efficiency. Finally, we showed that the m1 mRNA, which is transcribed very poorly in vivo, is translated very efficiently in vitro; and that its 5'-upstream sequence is as effective in increasing protein sigma 1 formation as that of s4 mRNA. Since both m1 mRNA and protein mu 2 are stable in infected cells, the reason why m1 mRNA is translated so inefficiently in vivo therefore remains unexplained.

Codon↗

CHO mutants resistant to colchicine, colcemid or griseofulvin have an altered beta-tubulin.

Single-step mutants of Chinese hamster ovary (CHO) cells have been isolated which are resistant to killing by the anti-mitotic drugs colchicine, colcemid or griseofulvin. Two-dimensional gel analysis showed that two mutants resistant to griseofulvin, one resistant to colcemid and one resistant to colchicine carry an alteration in the beta-tubulin subunit. Most of the remaining isolates are believed to be permeability mutants on the basis of their cross resistance to drugs which do not interefere with microtubular polymerization or function (Ling and Thompson, 1974; Bech-Hansen, Till and Ling, 1976). A reduced amount of the wild-type beta-tubulin protein remained in each of the beta-tubulin mutants, but a beta-tubulin protein with a more basic isoelectric point also appeared. Messenger RNAs coding for both wild-type and variant beta-tubulins were found in at least one mutant as assayed by in vitro translation in a reticulocyte lysate. This indicates that the altered tubulin does not arise as the result of a posttranslational modification.

Animals↗

Mannose-binding lectin: clinical implications for infection, transplantation, and autoimmunity.

Mannose-binding lectin (MBL) is a recognition molecule of the lectin pathway of complement and a key component of innate immunity. MBL variant alleles have been described in the coding region of the MBL gene, which are associated with low MBL serum concentration and impaired MBL structure and function. Both high and low serum levels of functional MBL have been associated with a variety of diseases and disease complications. Functioning as double-edged sword, low MBL serum levels have been shown to enhance the risk for infections. On the other hand, high MBL serum levels and high MBL activity have been associated with inflammatory diseases, transplant rejection, and diabetic nephropathy. Underscoring the Jekyll-and-Hyde character of MBL, both high and low serum MBL levels are associated with several aspects of autoimmune diseases. This review provides a general outline of the genetic and molecular characteristics of MBL and discusses MBL-disease association and its consequence in infection, transplantation, and autoimmunity.

Autoimmunity↗

No association of attention-deficit/hyperactivity disorder with genes of the serotonergic pathway in Han Chinese subjects.

Attention-deficit/hyperactivity disorder (ADHD) is a complex psychiatric syndrome with cardinal symptoms of inattention, hyperactivity and impulsivity, and is a significant risk factor for poor health outcomes in both adolescence and adulthood. Etiology is clearly multifactoral, with probable contributions from both genetic and environmental factors. The genetic contribution is prominent, with estimated heritability at about 0.80. Although effects in dopamine metabolism have long been implicated in the etiology of ADHD, the role for serotonin has gained more attention in recent years. The current study examined five variants in three serotonin genes [those that code for serotonin receptors 2A (HTR2A), 5A (HTR5A) and 6 (HTR6)] in a relatively large sample of ADHD nuclear families. The transmission disequilibrium test (TDT) and the extended transmission disequilibrium test (ETDT) were performed to test for evidence of distorted transmission of alleles or haplotypes. No significant biased transmission was observed. These results do not support a substantial role of these serotonin gene in ADHD, however, additional work may be warranted before this association is definitively discounted.

Asian People↗

Angiotensin II type 2 receptor gene is not responsible for familial vesicoureteral reflux.

PURPOSE: The renin-angiotensin system has an important role in the development of the kidney and ureter. It has been reported that disruption of the angiotensin II type 2 receptor (AT2) gene leads to congenital anomalies of the kidney and ureter in mice, including vesicoureteral reflux. In humans a single base A to G transition at position -1332 in intron 1 (A-1332G) of the AT2 gene has been reported to occur significantly more often in patients with ureteropelvic junction obstruction and primary obstructive megaureter than in controls. We investigate the incidence of A-1332G transition in patients with primary familial vesicoureteral reflux to determine if AT2 gene is involved in pathogenesis of this disease. MATERIALS AND METHODS: We evaluated the incidence of A-1332G transition in 82 male and 110 female patients, 111 male and 124 female nonaffected family members from 88 families in which 2 or more members had primary vesicoureteral reflux, and 106 male and 107 female controls with no unselected for reflux status. Genomic DNA was extracted from whole blood samples. Polymerase chain reaction method modified for fluorescent detection was used to type all samples for the A-1332G variant. Furthermore, to identify mutations in the coding sequence of the AT2 gene, we selected 61 patients from different families as well as 15 controls with no vesicoureteral reflux status. RESULTS: The incidence of A-1332G transition in male patients with primary familial vesicoureteral reflux and controls was 33% (27 of 82 patients) and 38% (41 of 106 controls), respectively, and, the incidence of A-1332G substituted allele in female patients and controls was 47% (104 of 220 total alleles) and 50% (107 of 214 total alleles), respectively. Moreover, the transmission/disequilibrium test revealed no significant skewing of genotype transmission from mother to children. None of the 61 patients or 15 controls carried by mutations or polymorphisms in the coding sequence of the AT2 gene. CONCLUSIONS: Although the AT2 gene has been reported to have a role in developmental anomalies of the kidney and ureter, our data indicate that it is not involved in the pathogenesis of primary familial vesicoureteral reflux.

Angiotensin II↗

Mutation analysis of the N-methyl-D-aspartate receptor NR1 subunit gene (GRIN1) in schizophrenia.

Dysfunction of N-methyl-D-aspartate (NMDA) type ionotropic glutamate receptors has been implicated in the etiology of schizophrenia based on psychotomimetic properties of the antagonist phencyclidine (PCP) and observation that mice expressing low levels of the N-methyl-D-aspartate receptor NR1 subunit exhibit behavioral alterations that may be ameliorated by neuroleptic drugs. Based on the hypothesis that some schizophrenic patients have functionally deficient mutation(s) of the gene encoding N-methyl-D-aspartate receptor NR1 subunit (GRIN1), we screened 48 Japanese patients with schizophrenia for mutations in the coding region of the GRIN1 gene. Four variants, IVS2-22T>C, IVS2-12G>A, IVS4-34C>T, and 1719G/A (Pro516Pro), were identified. No non-synonymous mutation was detected. No significant association was suggested by case-control comparisons. Results indicate that genomic variations of the GRIN1 gene are not likely to be involved substantially in the etiology of schizophrenia.

Adult↗

Effect of nucleotide substitutions in N-acetyltransferase-1 on N-acetylation (deactivation) and O-acetylation (activation) of arylamine carcinogens: implications for cancer predisposition.

Genetic polymorphism in N-acetyltransferase-1 (NAT1) is associated with increased risk of various cancers, but epidemiological investigations are compromised by poor understanding of the relationship between NAT1 genotype and phenotype. Human reference NAT1*4 and 12 known human NAT1 allelic variants possessing nucleotide polymorphisms in the NAT1 coding region were cloned and expressed in yeast (Schizosaccharomyces pombe). Large reductions in the N-acetylation of 4-aminobiphenyl and the O-acetylation of N-hydroxy-2-aminofluorene were observed for recombinant NAT1 allozymes encoded by NAT1*14B, NAT1*15, NAT1*17, NAT1*19, and NAT1*22. Each of these alleles exhibited substantially lower expression of NAT1 protein than the reference NAT1*4 and the other NAT1 alleles. These results show an important effect of the NAT1 genetic polymorphism on the N- and O-acetylation of arylamine carcinogens, suggesting modification of cancer susceptibility following exposures to arylamine carcinogens.

Acetylation↗